Porcine reproductive and respiratory syndrome virus(PRRSV)mainly causes sow abor-tion,stillbirth,mummified fetus and respiratory symptoms in piglets.Since first reported in China in 1996,the virus complexity has increased significantly in more than 20 years of genetic evolution,bringing huge economic losses to the pig industry.In recent years,with the emergence of various PRRSV recombinant virus strains,preventing and controlling this epidemic became increasingly difficult.The purpose of this article is to comprehensively review the genome structure and func-tion of PRRSV,RNA virus recombination mechanism,main types of recombination,and the epi-demic status and recombination for the dominant epidemic PRRSV strains,in order to provide clues for in-depth research on gene recombination of PRRSV,thus providing the theoretical sup-port for formulating scientific prevention and control strategies.

Porcine reproductive and respiratory syndrome virus(PRRSV)mainly causes sow abor-tion,stillbirth,mummified fetus and respiratory symptoms in piglets.Since first reported in China in 1996,the virus complexity has increased significantly in more than 20 years of genetic evolution,bringing huge economic losses to the pig industry.In recent years,with the emergence of various PRRSV recombinant virus strains,preventing and controlling this epidemic became increasingly difficult.The purpose of this article is to comprehensively review the genome structure and func-tion of PRRSV,RNA virus recombination mechanism,main types of recombination,and the epi-demic status and recombination for the dominant epidemic PRRSV strains,in order to provide clues for in-depth research on gene recombination of PRRSV,thus providing the theoretical sup-port for formulating scientific prevention and control strategies.

Objective:To investigate the effect of mannose on the radiosensitivity of six human non-small cell lung cancer cell lines and its possible mechanism.Methods:The expression of mannose phosphate isomerase in six lung cancer cell lines were detected by Western blot. The inhibitory effect of mannose on the proliferation of lung cancer cell lines were observed by MTT assay. When irradiated with 0, 2, 4, 6, 8 and 10 Gy, the effect of mannose on the radiosensitivity of six lung cancer cell lines was detected by plate clone formation assay, respectively; and the apoptosis rates of normal control, mannose, irradiation and combined groups were detected by flow cytometry.Results:The expression levels of mannose phosphate isomerase were different among six lung cancer cell lines. Among them, A549 cells had the highest expression level and H460 cells showed the lowest expression level. When aD ministrated with 11.1 mmol/L mannose, the same inhibitory effect was observed on both A549 and H460 cell lines. Moreover, the inhibitory effect on H460 cell line was significantly increased with the increase of mannose concentration. In addition, aD ministration of 11.1 mmol/L mannose could significantly increase the radiosensitivity and apoptosis rate of H460 cell line. However, it exerted limited effect upon the radiosensitivity and apoptosis rate of A549 cell line. Conclusion:In six lung cancer cell lines with high expression of mannose phosphate isomerase, the aD ministration of mannose can enhance the radiosensitivity of partial tumors cells.

To investigate the mutation site of pathogenic gene in patients with hypertrophic cardiomyopathy (HCM) and to analyze the relationship between the genotype and clinical phenotype. Methods: Targeted exon capture sequencing was conducted in a HCM proband for 30 coding exons related HCM gene by all exon amplification and high-throughput sequencing. Furthermore, Sanger sequencing was performed in other family member and in 200 healthy volunteers for verification. The familial investigation included in clinical presentation, physical examination, electrocardiogram and echocardiography. Results: There were 3/6 blood relatives carrying cardiac myosin-binding protein gene MyBPC3 G772A heterozygous mutation, the mutation site was at 258 amino acid of MyBPC3 as glutamic acid (Glu) was substitute to lysine (Lys), such mutation was not found in rest of family member and not in healthy volunteers. The onset of proband and her daughter was rather late, they had palpitation and chest tightness; echocardiography showed interventricular septum basal segment thickening (16-18) mm. Proband was complicating paroxysmal ventricular tachycardia, malignant arrhythmia and heart failure, the maximum pressure gradient of left ventricular outflow was 56 mmHg, which with the high risk for sudden death. Conclusion: Comprehensive gene test has been helpful for clinical stratification, early diagnosis and treatment. MYBPC3 site mutation c.G772A might be the pathogenic mutation in that specific HCM family.